Clinical Overview > Condition/ Syndrome > Diabetes mellitus type 2
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Search for other papers by Murray B Gordon in
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Search for other papers by Kellie L Spiller in
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Summary
Long-acting pasireotide is an effective treatment option for acromegaly, but it is associated with hyperglycemia, which could impact its use in patients with diabetes. We present a case of a 53-year-old man with acromegaly and type 2 diabetes mellitus (glycated hemoglobin (HbA1c): 7.5%), who refused surgery to remove a pituitary macroadenoma and enrolled in a Phase 3 clinical trial comparing long-acting pasireotide and long-acting octreotide in acromegalic patients. The patient initially received octreotide, but insulin-like growth factor 1 (IGF-1) levels remained elevated after 12 months (383.9 ng/mL; 193.0 ng/mL; reference range: 86.5–223.8 ng/mL), indicating uncontrolled acromegaly. He switched to pasireotide 40 mg and subsequently increased to 60 mg. Within 6 months, IGF-1 levels normalized (193.0 ng/mL), and they were mostly normal for the next 62 months of treatment with pasireotide (median IGF-1: 190.7 ng/mL). Additionally, HbA1c levels remained similar to or lower than baseline levels (range, 6.7% to 7.8%) during treatment with pasireotide despite major changes to the patient’s antidiabetic regimen, which included insulin and metformin. Uncontrolled acromegaly can result in hyperglycemia due to an increase in insulin resistance. Despite having insulin-requiring type 2 diabetes, the patient presented here did not experience a long-term increase in HbA1c levels upon initiating pasireotide, likely because long-term control of acromegaly resulted in increased insulin sensitivity. This case highlights the utility of long-acting pasireotide to treat acromegaly in patients whose levels were uncontrolled after long-acting octreotide and who manage diabetes with insulin.
Learning points
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Long-acting pasireotide provided adequate, long-term biochemical control of acromegaly in a patient with insulin-requiring type 2 diabetes mellitus who was unresponsive to long-acting octreotide.
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Glycemic levels initially increased after starting treatment with pasireotide but quickly stabilized as acromegaly became controlled.
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Long-acting pasireotide, along with an appropriate antidiabetic regimen, may be a suitable therapy for patients with acromegaly who also have insulin-requiring type 2 diabetes mellitus.
Search for other papers by Cliona Small in
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Search for other papers by Aoife M Egan in
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Search for other papers by El Muntasir Elhadi in
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Search for other papers by Michael W O’Reilly in
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Search for other papers by Aine Cunningham in
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Search for other papers by Francis M Finucane in
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Summary
We describe three patients presenting with diabetic ketoacidosis secondary to ketosis prone type 2, rather than type 1 diabetes. All patients were treated according to a standard DKA protocol, but were subsequently able to come off insulin therapy while maintaining good glycaemic control. Ketosis-prone type 2 diabetes (KPD) presenting with DKA has not been described previously in Irish patients. The absence of islet autoimmunity and evidence of endogenous beta cell function after resolution of DKA are well-established markers of KPD, but are not readily available in the acute setting. Although not emphasised in any current guidelines, we have found that a strong family history of type 2 diabetes and the presence of cutaneous markers of insulin resistance are strongly suggestive of KPD. These could be emphasised in future clinical practice guidelines.
Learning points:
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Even in white patients, DKA is not synonymous with type 1 diabetes and autoimmune beta cell failure. KPD needs to be considered in all patients presenting with DKA, even though it will not influence their initial treatment.
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Aside from markers of endogenous beta cell function and islet autoimmunity, which in any case are unlikely to be immediately available to clinicians, consideration of family history of type 2 diabetes and cutaneous markers of insulin resistance might help to identify those with KPD and are more readily apparent in the acute setting, though not emphasised in guidelines.
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Consideration of KPD should never alter the management of the acute severe metabolic derangement of DKA, and phasing out of insulin therapy requires frequent attendance and meticulous and cautious surveillance by a team of experienced diabetes care providers.
Search for other papers by Runa Acharya in
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University of Iowa, Carver College of Medicine, Iowa City, Iowa, USA
Medicine and Endocrinology, University of Iowa, Iowa City, Iowa, USA
Des Moines University, Des Moines, Iowa, USA
Search for other papers by Udaya M Kabadi in
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Summary
Diabetic ketoacidosis (DKA) is commonly encountered in clinical practice. The current case is a unique and rare presentation of DKA as the initial manifestation of Cushing’s disease secondary to ACTH-secreting pituitary adenoma. Appropriate management as elaborated in the article led to total remission of diabetes as well as the Cushing’s disease.
Learning points:
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DKA is a serious and potentially life-threatening metabolic complication of diabetes mellitus.
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Some well-known precipitants of DKA include new-onset T1DM, insulin withdrawal and acute illness.
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In a patient presenting with DKA, the presence of a mixed acid–base disorder warrants further evaluation for precipitants of DKA.
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We present a rare case of DKA as an initial manifestation of Cushing’s disease secondary to ACTH-producing pituitary adenoma.
Search for other papers by Ernesto Solá in
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Search for other papers by Carmen Rivera in
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Search for other papers by Michelle Mangual in
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Search for other papers by Kelvin Rivera in
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Search for other papers by Ricardo Fernandez in
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Summary
Diabetes mellitus was identified as a risk factor for developing tuberculosis (TB) infection, and relapse after therapy. The risk of acquiring TB is described as comparable to that of HIV population. The fact that diabetics are 3× times more prone to develop pulmonary TB than nondiabetics cannot be overlooked. With DM recognized as global epidemic, and TB affecting one-third of the world population, physicians must remain vigilant. We present a 45-year-old woman born in Dominican Republic (DR), with 10-year history of T2DM treated with metformin, arrived to our Urgency Room complaining of dry cough for the past 3months. Interview unveiled unintentional 15lbs weight loss, night sweats, occasional unquantified fever, and general malaise but denied bloody sputum. She traveled to DR 2years before, with no known ill exposure. Physical examination showed a thin body habitus, otherwise well appearing woman with stable vital signs, presenting solely right middle lung field ronchi. LDH, ESR, hsCRP and Hg A1C were elevated. Imaging revealed a right middle lobe cavitation. Sputum for AFB disclosed active pulmonary TB. Our case portrays that the consideration of TB as differential diagnosis in diabetics should be exercised with the same strength, as it is undertaken during the evaluation of HIV patients with lung cavitation. Inability to recognize TB will endanger the patient, hospital dwellers and staff, and perpetuate this global public health menace.
Learning points
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Diabetes mellitus should be considered an important risk factor for the reactivation of pulmonary tuberculosis.
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High clinical suspicious should be taken into consideration as radiological findings for pulmonary tuberculosis in patients with diabetes mellitus may be atypical, involving middle and lower lobes.
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Inability to recognize pulmonary tuberculosis will endanger the patient, hospital dwellers and staff, and perpetuate this global public health menace.
Department of Medicine, Waterbury Hospital, Waterbury, Connecticut, USA
Search for other papers by S M Kandel in
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Department of Medicine, Waterbury Hospital, Waterbury, Connecticut, USA
Search for other papers by J A Cosgriff in
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Summary
Clinicians are often presented with the scenario of what to do when one medication in a drug class has failed a therapeutic trial on a patient. We encountered a patient who developed profound resistance to glargine, aspart and regular insulin, but had a rapid and sustained response to detemir. The mechanism of the increased sensitivity to detemir is unclear, but may be related to an additional carbon chain on detemir shielding it from an antibody response. This case highlights the profound impact that subtle differences in molecular structure can have on biological activity and thus patient outcomes.
Learning points
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Subtle differences in molecular structure can have a profound impact on biological activity, and thus patient outcomes.
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Poor outcomes with one medication in a drug class should not be used to rule out the efficacy of all related medications.
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Detemir has been shown to be less immunogenic than other insulins, and should be considered in patients with insulin resistance.
Search for other papers by Alessandro Mantovani in
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Search for other papers by Maddalena Trombetta in
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Search for other papers by Federica Zamboni in
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Search for other papers by Massimiliano Bruti in
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Search for other papers by Giorgio Ravenna in
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Search for other papers by Fabrizia Perrone in
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Search for other papers by Vincenzo Stoico in
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Search for other papers by Enzo Bonora in
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Summary
Vertebral osteomyelitis (or spondylodiscitis) is steadily increasing in Western countries and often results from hematogenous seeding, direct inoculation during spinal surgery, or contiguous spread from an infection in the adjacent soft tissue. We present the case of a 67-year-old white patient with type 2 diabetes who went to Hospital for high fever, back pain, and worsening of known infected ulcers in the left foot. Despite intravenous antibiotic treatment and surgical debridement of the foot infection, high fever and lower back pain continued. Bone biopsy and two consecutive blood cultures were positive for Staphylococcus aureus. A spinal magnetic resonance imaging (MRI) was performed, revealing serious osteomyelitis in L4 and L5 complicated by an epidural abscess. Contiguous or other distant focuses of infection were not identified. In this case, diabetic foot could be considered as a primary distant focus for vertebral osteomyelitis. Clinicians should consider vertebral osteomyelitis as a ‘possible’ diagnosis in patients with type 2 diabetes complicated by foot infection that is associated with fever and lower back pain.
Learning points
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Vertebral osteomyelitis is increasing in Western countries, especially in patients with type 2 diabetes.
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The primary focus of infection is the genitourinary tract followed by skin, soft tissue, endocarditis, bursitis, septic arthritis, and intravascular access.
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Diabetic foot could be a rare primary focus of infection for vertebral osteomyelitis, and, however, vertebral osteomyelitis could be a serious, albeit rare, complication of diabetic foot.
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Clinicians should keep in mind the many potential complications of diabetic foot ulcerations and consider vertebral osteomyelitis as a “possible” diagnosis in patients with type 2 diabetes and foot ulcers associated with nonspecific symptoms such as lower back pain.
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Early diagnosis and correct management of vertebral osteomyelitis are crucial to improve clinical outcomes.
Search for other papers by Benjamin G Challis in
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Search for other papers by Chung Thong Lim in
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Search for other papers by Alison Cluroe in
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Search for other papers by Ewen Cameron in
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Search for other papers by Stephen O’Rahilly in
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Summary
McKittrick–Wheelock syndrome (MWS) is a rare consequence of severe dehydration and electrolyte depletion due to mucinous diarrhoea secondary to a rectosigmoid villous adenoma. Reported cases of MWS commonly describe hypersecretion of mucinous diarrhoea in association with dehydration, hypokalaemia, hyponatraemia, hypochloraemia and pre-renal azotemia. Hyperglycaemia and diabetes are rarely reported manifestations of MWS. Herein we describe the case of a 59-year-old woman who presented with new-onset diabetes and severe electrolyte derangement due to a giant rectal villous adenoma. Subsequent endoscopic resection of the tumour cured her diabetes and normalised electrolytes. This case describes a rare cause of ‘curable diabetes’ and indicates hyperaldosteronism and/or whole-body potassium stores as important regulators of insulin secretion and glucose homeostasis.
Learning points
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McKittrick–Wheelock syndrome (MWS) is typically characterised by the triad of pre-renal failure, electrolyte derangement and chronic diarrhoea resulting from a secretory colonic neoplasm.
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Hyperglycaemia and new-onset diabetes are rare clinical manifestations of MWS.
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Hyperaldosteronism and/or hypokalaemia may worsen glucose tolerance in MWS.
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Aggressive replacement of fluid and electrolytes is the mainstay of acute management, with definitive treatment and complete reversal of the metabolic abnormalities being achieved by endoscopic or surgical resection of the neoplasm.
Search for other papers by Arshpreet Kaur in
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Search for other papers by Stephen J Winters in
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Summary
Drugs that inhibit the sodium-glucose co-transporter-2 (SGLT2) are an exciting novel, insulin-independent treatment for diabetes that block glucose reabsorption from the proximal tubules of the kidney, leading to increased glucose excretion and lower blood glucose levels. Inhibition of SGLT2 activity also reduces sodium reabsorption, which together with glycosuria produces a mild diuretic effect with the potential for dehydration and hyperkalemia. We report on a 60-year-old man with uncontrolled type 2 diabetes treated with insulin, glimepiride, metformin and canagliflozin, who was admitted with altered mental status after a syncopal episode. He had a 1-week history of ingestion of Tums for heartburn followed by poor appetite and lethargy. Laboratory work-up showed acute kidney injury, diabetic ketoacidosis (DKA), and parathyroid hormone-independent severe hypercalcemia of 17.4 mg/dl. DKA resolved with insulin treatment, and saline hydration led to improvement in hypercalcemia and renal function over 48 h, but was accompanied by a rapid increase in the serum sodium concentration from 129 to 162 mmol/l despite changing fluids to 0.45% saline. Urine studies were consistent with osmotic diuresis. Hypernatremia was slowly corrected with hypotonic fluids, with improvement in his mental status over the next 2 days. This is the first report of hypercalcemia associated with the use of a SLGT2 inhibitor. Although the exact mechanism is unknown, canagliflozin may predispose to hypercalcemia in patients ingesting excessive calcium because of dehydration from osmotic diuresis, with reduced calcium excretion and possible increased intestinal calcium absorption. Saline therapy and osmotic diuresis may lead to hypernatremia from electrolyte-free water loss.
Learning points
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Canagliflozin, an SGLT2 inhibitor, may cause hypercalcemia in susceptible patients.
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Although the exact mechanisms are unknown, dehydration from osmotic diuresis and increased intestinal calcium absorption play a role.
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Close monitoring of serum calcium levels is recommended in patients treated with SGLT2 inhibitors who are elderly, have established hypercalcemia, or take oral calcium supplements.
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Saline therapy and osmotic diuresis may lead to hypernatremia from electrolyte-free water loss in susceptible patients.
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Search for other papers by David V Morris in
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Search for other papers by Michael H Dahan in
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Summary
Cerebral vascular accidents are caused by vasospasm when induced by preeclampsia or by dopamine agonists. However, six arteries nourish the pituitary and prevent against vasospasm-induced damage, which up until now has not been thought to occur. Bromocriptine was used to arrest lactation in a 31-year-old with secondary amenorrhea following preeclampsia and fetal demise at 28 weeks gestation. Tests and history revealed panhypopituitarism not associated with hemorrhage or mass infarction but instead caused by vasospasm. The present study is the first report of pituitary damage from a non-hemorrhagic, vaso-occlusive event in the literature. In keeping with Sheehan's and Simon's syndromes, we have named pituitary damage resulting from vaso-occlusion as Dahan's syndrome, and a literature review suggests that it may be a common and previously overlooked disorder.
Learning points
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Vasospasm can cause damage to the pituitary gland, although it was not previously believed to do so.
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Preeclampsia and the use of a dopamine agonist, particularly in the peripartum state, may trigger vasospasm.
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Vasospasm resulting from dopamine agonists may be a common cause of injury to the pituitary gland, and it may have been overlooked in the past.
Search for other papers by Soham Mukherjee in
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Search for other papers by Kim Vaiphei in
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Search for other papers by Pinaki Dutta in
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Summary
Spontaneous diabetic muscle infarction (DMI) is a rare and under diagnosed complication of diabetes mellitus. Clinically it presents with acute to subacute onset swelling, pain and tenderness of muscle(s) without systemic manifestations. MRI is helpful in diagnosis, exclusion of other causes and for localization of affected muscle for biopsy in atypical cases. Muscles of the thighs are commonly affected in diabetic myonecrosis (DMN). Here we present the summary of four cases seen in the last 3 years in a tertiary care centre with simultaneous or sequential involvement of multiple groups of muscles or involvement of uncommon sites. All these patients had advanced duration of diabetes with microvascular complications and poor glycemic control. Conservative management including rest and analgesics is the treatment of choice. Short-term prognosis is good but there may be recurrence.
Learning points
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A high index of suspicion is required for the diagnosis of DMN which can avoid inadvertent use of antibiotics.
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Acute–subacute onset severe focal muscle pain in the absence of systemic symptoms in a female patient with long-standing diabetes with microvascular complications suggests DMI.
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MRI is the most sensitive test for diagnosis.
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Muscle biopsy should be reserved for atypical cases.
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Conservative management including rest and analgesics has good outcome.
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Improvement usually occurs within 6–8 weeks, but there may be recurrence.